26 yo F with SLE, SLE nephritis (mesangioproliferative), has low C3, Low C4. Anti-smith was positive. Anti- DNA is 1: 320 (used to be 1:640). Had been on chronic steroids and has bilateral hip pain due to early AVN. Was on Cellcept, which was discontinued due to pancytopenia. Thiopurine Methyltransferase level is 22.2 (normal: 25-65). How do you manage the patient. She has had sub-acute skin lesions as well. You diagnose the paitent with moderate activity of SLE. She has received BCG vaccination as a child.

the deformities result mainly from soft-tissue abnormalities, such as laxity of ligaments, fibrosis of the capsule, and muscular imbalance, rather than from destruction of the bone of joints, as occurs in rheumatoid arthritis. The mainstay of the management of Jaccoud’s arthropathy includes physical therapy and the use of orthotic devices

The ‘cytokine shift’
hypothesis proposes that pharmacological systemic blockade of
TNF-alpha suppresses production of Th1 cytokines, thereby driving
the immune response towards Th2 cytokine production, IL-10
and IFN-alpha. This change in cytokine balance would then induce
a cascade of downstream events ultimately resulting in production
of the autoantibodies and a lupus-like syndrome.

Apoptosis Hypothesis

Another hypothesis is based on the assumption that systemic
inhibition of TNF-alpha could interfere with apoptosis, affect the clearance of nuclear debris and thus promote autoantibody production against DNA and other nuclear antigens.

Similarly, TNF-alpha-induced apoptosis of mature cytotoxic T cells is
an important mechanism for termination of T lymphocyte-driven
responses. Anti-TNF-alpha therapy may interfere with this process
and thereby promote autoantibody formation against nuclear
antigens.

Some nuclear antigens, namely nucleosomes, become detectable
in the plasma of RA patients after the start of anti-TNF-alpha therapy. Interestingly, such a rise in plasma nucleosome levels might
contribute to a break of tolerance and thereby induce autoantibodies in susceptible individuals. This notion is supported
by a recent study, which found that the occurrence of anti-
nucleosome antibodies correlated strongly with the presence
of ANA in anti-TNF-alpha-treated RA patients.

45 yo M patient is seen for Acute on Chronic Renal Failure. CMP is as follow.

UA is as below. USG showed no obstruction. Ur - E was normal

Spot Ur-Pr/Cr is as follow.

Patient was diagnosed previously of SLE with Nephritis. Unknown what pathological diagnosis patient had. However, was on Cellcept since diagnosis of SLE with Nephritis in 2014. Rheumatological work up revealed the following.

Renal Biopsy is Done because of the worsening AKI. Before we discuss the findings of the biopsy, what are the renal manifestation of SLE?